{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,14]],"date-time":"2025-05-14T02:08:48Z","timestamp":1747188528795,"version":"3.40.5"},"reference-count":29,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2019,12,26]],"date-time":"2019-12-26T00:00:00Z","timestamp":1577318400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000023","name":"Government of Canada","doi-asserted-by":"publisher","award":["EQPEQ0407690\u201011"],"award-info":[{"award-number":["EQPEQ0407690\u201011"]}],"id":[{"id":"10.13039\/501100000023","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000038","name":"Natural Sciences and Engineering Research Council of Canada","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000038","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>The immediate increase in skeletal muscle blood flow following contraction is greater when the contracting muscle is below <jats:italic>vs<\/jats:italic>. above heart level. This has been attributed to muscle pump\u2010mediated venous emptying and subsequent widening of the arterial to venous pressure gradient, which can occur below but not above heart level.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>However, alternative explanations could include greater rapid onset vasodilatation and\/or transmural pressure\u2010mediated mechanical distension of resistance vessels, but these remain unexplored.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We demonstrate that active vasodilatation is not responsible for greater post\u2010contraction hyperaemia below the heart. Instead, an increased transmural pressure\u2010mediated mechanical distension of resistance vessels is a key mechanism responsible for this phenomenon.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Our findings establish the importance of considering\/accounting for local mechanical arteriolar distension effects when investigating exercise hyperaemia.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>They also inform the application of exercise for rehabilitative purposes and prompt investigation into whether arteriolar distension accompanying vasodilatation is reduced with diseases or ageing, thereby compromising exercising muscle perfusion.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p>We tested the hypotheses that increased post\u2010contraction hyperaemia in higher (H; below heart) <jats:italic>vs<\/jats:italic>. lower (L; above heart) transmural pressure conditions is due to (1) greater active vasodilatation or (2) greater transmural pressure\u2010mediated arteriolar distension. Participants (<jats:italic>n<\/jats:italic>\u00a0=\u00a020, 12 male, 8 female; combined mean age 24.5\u00a0\u00b1\u00a02\u00a0years) performed a 2\u00a0s isometric handgrip contraction, where arm position was maintained within or changed between H and L during contraction, resulting in four starting\u2013finishing arm position conditions (LL, HL, LH, HH). Post\u2010contraction forearm blood flow (echo and Doppler ultrasound) was higher with contraction release in H <jats:italic>vs<\/jats:italic>. L environments (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05). However, contraction initiated in H did not result in greater vasodilatation (forearm vascular conductance; FVC) than contraction initiated in L, regardless of contraction release condition (peak FVC: LL 217\u00a0\u00b1\u00a0104 <jats:italic>vs<\/jats:italic>. HL 204\u00a0\u00b1\u00a092\u00a0ml min<jats:sup>\u22121<\/jats:sup> (100\u00a0mmHg)<jats:sup>\u22121<\/jats:sup>, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.313, LH 229\u00a0\u00b1\u00a08 <jats:italic>vs<\/jats:italic>. HH 225\u00a0\u00b1\u00a085\u00a0ml min<jats:sup>\u22121<\/jats:sup> (100\u00a0mmHg)<jats:sup>\u22121<\/jats:sup>, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.391; first post\u2010contraction cardiac cycle FVC: same comparisons, both <jats:italic>P<\/jats:italic>\u00a0=\u00a00.317). However, FVC of the first post\u2010contraction cardiac cycle was greater for contractions released in H <jats:italic>vs<\/jats:italic>. L regardless of pre\u2010contraction condition (LL 106\u00a0\u00b1\u00a067 <jats:italic>vs<\/jats:italic>. LH 152\u00a0\u00b1\u00a076\u00a0ml min<jats:sup>\u22121<\/jats:sup> (100\u00a0mmHg)<jats:sup>\u22121<\/jats:sup>, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05; HL 80\u00a0\u00b1\u00a051 <jats:italic>vs<\/jats:italic>. HH 119\u00a0\u00b1\u00a058\u00a0ml min<jats:sup>\u22121<\/jats:sup> (100\u00a0mmHg)<jats:sup>\u22121<\/jats:sup>, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05). These findings refute the hypothesis that greater hyperaemia following a single contraction in higher transmural pressure conditions is due to greater active vasodilatation. Instead, our findings reveal a key role for increased transmural pressure\u2010mediated mechanical distension of arterioles in creating a greater increase in vascular conductance for a given active vasodilatation following skeletal muscle contraction.<\/jats:p><\/jats:sec>","DOI":"10.1113\/jp278476","type":"journal-article","created":{"date-parts":[[2019,10,26]],"date-time":"2019-10-26T00:09:09Z","timestamp":1572048549000},"page":"85-99","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Greater post\u2010contraction hyperaemia below <i>vs<\/i>. above heart level: the role of active vasodilatation <i>vs<\/i>. passive mechanical distension of arterioles"],"prefix":"10.1113","volume":"598","author":[{"given":"Mytchel J. 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